Normal insulin production and regulation of blood glucose is a critical aspect of proper homeostasis. In humans, insulin is synthesized in the β cells of the islets of Langerhans in the pancreas, and is generally responsible for regulating carbohydrate metabolism. Specific cellular effects of insulin include increased fatty acid synthesis, decreased lipolysis, and increased glycogen synthesis. Defects in insulin production may result in various metabolic diseases, such as type 1 diabetes, in which insulin production is acutely impaired as a result of autoimmune pancreatic β cell destruction.
The regulation of blood glucose levels by insulin is achieved mainly by increased glucose transport into adipose and skeletal muscle tissue. The mechanism of glucose transport activation by insulin is the hormone-dependent enhancement of GLUT4 translocation from intracellular storage vesicles to the plasma membrane. Glucose uptake is increased proportionally to the increment of GLUT4 molecules in the plasma membrane. Insulin-responsive glucose transport is essential to the normal functioning and metabolism of fat and muscle tissue in normal human subjects. Insulin resistance of, for example, skeletal muscle glucose transport is a key defect in the development of metabolic diseases such as impaired glucose tolerance and type 2 diabetes.
A more detailed understanding of the molecular mechanisms responsible for insulin production and insulin-responsive glucose transport would greatly facilitate the development of therapeutic strategies aimed at modulating various metabolic diseases. In particular, the intracellular pathways and their respective molecules involved in such metabolic diseases serve as useful targets for treating metabolic diseases.